国际妇产科学杂志

国际妇产科学杂志 ›› 2019, Vol. 46 ›› Issue (3): 259-262.

• 论著 • 上一篇    下一篇

双酚A激活PI3K/AKT通路促进子宫内膜癌细胞增殖的研究

刘大江，杨媛，刘畅，杨永秀   

  1. 730000 兰州大学第一医院妇产科（刘大江，刘畅，杨永秀）；兰州大学第一医院生殖医学专科医院（杨媛）
  • 收稿日期:2018-11-19 修回日期:2019-03-14 出版日期:2019-06-15 发布日期:2019-06-25
  • 通讯作者: 杨永秀，E-mail：yongxiuyang@163.com E-mail:yongxiuyang@163.com;yangyongxiu2018@163.com
  • 基金资助:
    甘肃省科技计划项目（18JR3RA340）；兰州市科技计划项目（2017-4-56）；2017年兰州大学第一医院院内基金项目（ldyyn2017-01，ldyyn2017-13）

Bisphenol A Induced Endometrial Cancer Cell Proliferation by Activating PI3K/AKT Pathway

LIU Da-jiang，YANG Yuan，LIU Chang，YANG Yong-xiu   

  1. Department of Obstetrics and Gynecology，The First Hospital of Lan Zhou University，Lanzhou 730000，China（LIU Da-jiang，LIU Chang，YANG Yong-xiu）；Reproductive Medicine Hospital of the First Hospital of Lanzhou University，Lanzhou 730000，China（YANG Yuan）
  • Received:2018-11-19 Revised:2019-03-14 Published:2019-06-15 Online:2019-06-25
  • Contact: YANG Yong-xiu，E-mail：yongxiuyang@163.com E-mail:yongxiuyang@163.com;yangyongxiu2018@163.com

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摘要： 目的：研究双酚A（bisphenol A，BPA）活化磷脂酰肌醇3激酶/蛋白激酶B（PI3K/AKT）促子宫内膜癌细胞Ishikawa和RL952增殖的机制。方法：CCK8试剂盒检测Ishikawa和RL952细胞的增殖情况，蛋白质印迹（Western blotting）法检测p-AKT蛋白的表达。结果：在Ishikawa和RL952细胞中，BPA作用48 h时，细胞增殖呈浓度依赖性，1 μmol/L的BPA促细胞生长效应最显著，Ishikawa和RL952细胞增殖率分别为0.758±0.023和0.692±0.042。BPA浓度超过1 μmol/L后，促细胞增殖的作用下降。BPA作用24 h时促增殖效应不明显，BPA作用72 h时表现出细胞毒作用。1 μmol/L BPA处理的Ishikawa和RL952细胞48 h后p-AKT蛋白的表达较对照组升高（P＜0.05），加入PI3K抑制剂（LY294002），p-AKT的蛋白表达比对照组降低，但差异无统计学意义（P＞0.05）。结论：BPA通过激活PI3K/AKT通路促进子宫内膜癌细胞增殖。

关键词: 子宫内膜肿瘤, 磷酸肌醇3-激酶, 细胞增殖, 双酚A

Abstract: Objective：To explore the mechanism of bisphenol A on the proliferation in human endometrial cancer cells (Ishikawa and RL952) via PI3K/AKT signaling pathway. Methods：CCK8 assay was used to detect the proliferation in Ishikawa and RL952 cells, and Western blotting was applied to observe the expression of phosphorylation-AKT. Results：Ishikawa and RL952 cells proliferation increased significantly with treatment of 1 μmol/L BPA after 48 h, and cell proliferation was (0.758±0.023) and (0.692±0.042) respectively (P＜0.01). The proliferation effect decreased when BPA was more than 1 μmol/L. Ishikawa and RL952 cells did not increase after treated for 24 h. Cytotoxic effects were showed after BPA treated for 72 h. After 1 μmol/L BPA treated for 48 h, p-AKT expression was increased significantly compared with controls（P＜0.05）. When PI3K was blocked by LY294002, p-AKT expression was decreased, but it is not significant compared to controls (P＞0.05). Conclusions：Bisphenol A induced endometrial cancer cell proliferation by activating PI3K/AKT pathway.

Key words: Endometrial neoplasms, Phosphatidylinositol 3-kinase, Cell proliferation, Bisphenol A